Previous studies have shown that oxygen lowers the cardiac output and increases the SVR in normal persons. In addition, recent work indicates that oxygen has these same effects in patients with congestive heart failure (CHF) without altering the activity of the sympathetic nervous system (SNS). These findings led us to study whether oxygen had an effect on forearm vasodilator capacity during reactive hyperemia. We performed this study in normal subjects and in subjects with conditions that simulated congested heart failure -- sympathetic nervous system activation and venous congestion. We concluded that oxygen decreases the vasodilation that is normally seen after reactive hyperemia, and conditions of heart failure compound this effect. We hypothesized that the peripheral destruction of nitric oxide (NO) by oxygen mediates these effects. The effects of the increased SNS activation, increased angiotensin II and edema in CHF are partially counteracted by the actions of NO. NO has been found to be important in mediating the vasodilatory response in reactive hyperemia, but not in active hyperemia in normal subjects. Impairment of endothelium-dependent peripheral vasodilation is found in patients with CHF. However, it is unclear what role NO plays in this impairment. NO may compensate for the neurohumoral adaptations in CHF, so destruction of NO by oxygen may explain the adverse hemodynamic and vasoconstrictive effects of oxygen that was found in our previous studies. To answer whether destruction of NO by oxygen is a contributing mechanism to our observations and to determine whether subjects with CHF adapt to increased oxygen, we propose to administer 40% oxygen to subjects with stable CHF for eight hours. We will measure plasma nitrite, forearm blood flow after reactive hyperemia, and blood pressure before oxygen, 15 minutes later, at 3 hours, 6 hours and 8 hours. We hypothesize that 1) plasma nitrite levels will rise over time as oxygen destroys NO and NO synthase is induced ; 2) forearm vasodilator response will be impaired for the entire 8 hours of oxygen administration and 3) blood pressure may remain elevated in response to destruction of NO. These findings will be important because current management of hospitalized patients with CHF includes oxygen therapy. If our hypotheses are correct, the use of supplemental oxygen therapy in the absence of hypoxia may not be prudent because oxygen destroys one of the last remaining vascular adaptive responses in persons with CHF.